Deletion of virulence associated genes from attenuated African swine fever virus isolate OUR T88/3 decreases its ability to protect against challenge with virulent virus

被引：95
|
作者：
Abrams, Charles C. [1 ]
Goatley, Lynnette [1 ]
Fishbourne, Emma [1 ]
Chapman, David [1 ]
Cooke, Lyndsay [1 ]
Oura, Christopher A. [1 ]
Netherton, Christopher L. [1 ]
Takamatsu, Haru-Hisa [1 ]
Dixon, Linda K. [1 ]
机构：
[1] Pirbright Inst, Woking GU24 0NF, Surrey, England
来源：
VIROLOGY | 2013年 / 443卷 / 01期
基金：
英国生物技术与生命科学研究理事会;
关键词：
African swine fever virus; Attenuation; Virulence; CATALYTIC SUBUNIT; E3L GENE; VACCINE; GENOME; IMMUNIZATION; REPLICATION; PERSISTENCE; DETERMINANT; MATURATION; SIMILARITY;
D O I：
10.1016/j.virol.2013.04.028
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
African swine fever virus (ASFV) causes an acute haemorrhagic disease of domestic pigs against which there is no effective vaccine. The attenuated ASFV strain OUR T88/3 has been shown previously to protect vaccinated pigs against challenge with some virulent strains including OUR T88/1. Two genes, DP71L and DP96R were deleted from the OUR T88/3 genome to create recombinant virus OUR T88/3 Delta DP2. Deletion of these genes from virulent viruses has previously been shown to reduce ASFV virulence in domestic pigs. Groups of 6 pigs were immunised with deletion virus OUR T88/3 Delta DP2 or parental virus OUR T88/3 and challenged with virulent OUR T88/1 virus. Four pigs (66%) were protected by inoculation with the deletion virus OUR T88/3 Delta DP2 compared to 100% protection with the parental virus OUR T88/3. Thus the deletion of the two genes DP71L and DP96R from OUR T88/3 strain reduced its ability to protect pigs against challenge with virulent virus. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
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收藏
页码：99 / 105
页数：7
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